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作 者:李武全[1] 邱啸臣[2] 金以超[1] 葛茂星[1] 刘军[1] 夏照帆[2]
机构地区:[1]昆明医科大学第二附属医院烧伤科,昆明650101 [2]第二军医大学长海医院烧伤科,上海200433
出 处:《广东医学》2012年第13期1873-1875,共3页Guangdong Medical Journal
基 金:云南省卫生科技计划项目(编号:2009NS084)
摘 要:目的探讨山莨菪碱对烫伤后脑组织保护作用及其可能机制。方法 25只雄性SD大鼠随机分为假烫组(n=5)、烫伤组(n=10)和实验组(n=10)。实验组于建模成功后5 min给予山莨菪碱3 mg/kg,而烫伤组则于伤后5 min给予等体积的生理盐水,给药方式均腹腔内注射。其中烫伤组和实验组分别于伤后6、12 h后处死大鼠,采集脑组织。应用Western blot检测脑组织P-HSF-1和热休克蛋白70(HSP70)的表达,利用TUNNEL法检测细胞凋亡。结果烫伤组和实验组的凋亡细胞数在6、12 h较假烫组明显增高,实验组凋亡细胞数在6、12 h明显低于烫伤组(P<0.05);与烫伤组比较,6、12 h实验组脑组织P-HSF-1和HSP70的表达明显增强。结论山莨菪碱可能通过增强严重烫伤大鼠脑组织HSP70的表达来减轻烫伤后脑细胞凋亡。山莨菪碱能够促进脑组织HSF-1的磷酸化可能是其诱导HSP70表达的机制之一。Objective To investigate the protective effects of anisodamine on rats with severe burns. Methods Twenty five male SD rats were randomly divided into three groups: sham group (n =5) , burn injury group (n = 10) and anisodamine treatment group (n = 10). At 5 min after burn injury, anisodamine (3 mg/kg) was administered in the ani- sodaminc treatment group. In the burn injury group, the same volume of physiological saline was administered. In all the two groups, the route of administration was intraperitoneal injection. Each 5 rats in burn injury group and anisodamine treatment group were sacrificed at 6 and 12 h post - injury for cerebral samples investigation. P - HSF - 1 and HSP70 were detected using Western blot. TdT - mediated UTP - biotin nick end labeling (TUNEL) assay was used to assess the cerebral cell apoptosis. Results Burn injury resulted in rapidly significantly increase of cerebral cell apoptosis in both burn injury group and anisodamine treatment group at 6 and 12 h post - injury ( P 〈 O. 05 ). However, anisodamine treatment significantly reduced the burn injury - induced cerebral cell apoptosis at both 6 and 12 h post - burn injury. Furthermore, anisodamine treatment also resulted in significantly higher expression of P - HSF - 1 and HSP70 at the 6 and 12 h post - burn injury. Conclusion Anisoamine treatment induces up - regulation of HSPT0, which is probably mediated with HSF - 1 phosphorylation, thus alleviates the severe burn - induced cerebral cell apoptosis.
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